Interferon-αElicits Downregulation of Human Papillomavirus 18 mRNA in HeLa Cells by Selective Repression of Endogenous Viral Transcription

Perea, Silvio E.; López-Ocejo, Omar; García-Milián, Rolando; Araña, Manuel de J.

doi:10.1089/jir.1995.15.495

Cited by 11 publications

(4 citation statements)

References 29 publications

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“…IFN-␣ also inhibits HPV-16 E7 protein expression but not transcription and not E6 protein expression, suggesting that growth and transformation inhibition is mediated by an inhibition in E7 protein expression. Others (101,112) have shown that IFN-␣ inhibits transcription of HPV-18 E6 and E7 genes in HeLa cells, a cervical carcinoma cell line containing integrated HPV-18 DNA. Interestingly, this effect appears to be shared with IFN-␥ (101).…”

Section: School Of Medicine University Of California San Francisco mentioning

confidence: 99%

Cell-Mediated Immune Response to Human Papillomavirus Infection

Scott

Nakagawa

Moscicki

2001

Clin Diagn Lab Immunol

234

217

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Acquisition of human papillomavirus (HPV) results in an infection of variable duration which may or may not be associated with clinically apparent lesions. Lesions caused by skintropic HPV types generally manifest as cutaneous warts and most often resolve over a period of months to years. On the other hand, anogenital infections are more likely to remain clinically inapparent. The development of DNA amplificationbased tests has demonstrated that anogenital infections are quite common and generally self-limited. For example, we and others have shown by PCR testing of multiple samples collected at different points in time-that 70 to 90% of sexually active adolescents and young women who develop an incident cervical HPV infection will show clearance of infection within 12 to 30 months (47,61,94). The factors influencing the natural history of these infections are not well understood. Given that persistent anogenital infection with oncogenic HPV types is associated with increased risk of neoplasia and invasive cancers (22,59,70,71,94,124) and that cervical carcinoma remains a leading cause of death among women in developing countries (129), understanding these factors is of considerable importance.Substantial effort has been directed recently at understanding the role of the host's immune response in the natural history of HPV, and in particular, anti-viral, cell-mediated immunity. Empirical evidence for the importance of cell-mediated immunity in control of HPV infection comes from an extensive body of literature documenting the increased prevalence of HPV infection and associated disease among immunosuppressed populations, including those with iatrogenic immunosuppression such as renal transplant recipients and individuals with human immunodeficiency virus (HIV) infection. Sillman and coauthors (128) reported in 1984 on 20 immunosuppressed women with various causes of immunosuppression who had lower genital neoplasia, describing evidence of associated HPV infection in all 20. Penn, in 1986, reported a 100-fold increase in cancer of the vulva and anus in renal transplant recipients (111). In the 1990s, as molecular testing for HPV infection came into its own, several reports confirmed increased incidence of HPV infection (50) and associated morbidities, including warts (77) and cervical squamous intraepithelial lesions (SIL) (104), among immunosuppressed renal transplant recipients.The most persuasive evidence for the association between cellular immune defects and HPV infection and related morbidities comes from persons with HIV infection. Such individuals show increased prevalence of anogenital HPV infection (31, 32, 60, 105-107) as well as longer periods of HPV persistence (31,40,46,90,136). In addition, infection with multiple HPV types and with oncogenic types are more common (9,31,46,78,90,107,136). Associations between markers of HIV disease status (e.g., viral load and CD4 lymphocyte count) and HPV infection have been inconsistent. Most studies have suggested that advanced disease and greater immunological ...

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Section: School Of Medicine University Of California San Francisco mentioning

confidence: 99%

Cell-Mediated Immune Response to Human Papillomavirus Infection

Scott

Nakagawa

Moscicki

2001

Clin Diagn Lab Immunol

234

217

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“…Another study conducted on HeLa cells also suggested that 1 × 10 3 IU/mL IFN-α selectively inhibited cytoplasmic HPV 18 mRNA [68]. These results were confirmed by Perea et al, who even suggested that, as IFN-α did not affect HPV 18 transcripts stability nor did mediate its inhibitory effects through HPV 18 enhancer sequences, it could, however, possibly repress nascent viral transcripts through regulatory cellular flanking regions [69]. Nonetheless, our pilot data can open the way to further investigations on this HPV-specific active substance of 2LPAPI.…”

Section: Discussionmentioning

confidence: 67%

The Micro-Immunotherapy Medicine 2LPAPI® Displays Immune-Modulatory Effects in a Model of Human Papillomavirus Type-16 L1-Protein Capsid-Treated Human Peripheral Blood Mononuclear Cells and Antiproliferative Effects in a Model of Cervical Cancer Cells

Jacques,

Marchand,

Chatelais

et al. 2024

Cancers

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Human papillomavirus (HPV) is the second most common infectious agent causing cancer. Persistent infection with high-risk (HR)-HPV can lead to cervical intra-epithelial neoplasia and cervical carcinomas (CC). While host immune response is necessary for viral clearance, chronic immune activation contributes to a low-grade inflammation that can ultimately lead to carcinogenesis. The micro-immunotherapy medicine (MIM) 2LPAPI® could be a valuable tool to manage the clearance of the virus and reduce the risk of developing CC. In this in vitro study, we aimed to investigate its mode of action. We showed that actives from the MIM increased the IL-6, IFN-γ, and IP-10 secretion in human peripheral blood mononuclear cells (PBMCs) exposed to peptides derived from the HPV-16 capsid (HPV16(L1)). This could reflect an increase in the immune activity toward HPV-16. At the same time, some active substances reduced the lympho-proliferation and the expression of T-cell activation markers. Finally, some of the MIM actives displayed antiproliferative effects in CC-derived HeLa cells under serum-starvation conditions. Altogether, this body of data highlighted for the first time the dual effect of MIM in the framework of HR-HPV infections as a potential (i) immune modulator of HPV16(L1)-treated PBMCs and (ii) antiproliferative agent of HPV-positive CC cells.

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“…IFN also induces the MX proteins which directly interfere with viral replication (30). Both type I and II IFNs inhibit expression of E6 and E7 RNAs in HPV-immortalized cells (32)(33)(34)(35)(36)(37). IFN-alpha also inhibits immortalization of keratinocytes by HPV-16 (34).…”

Section: Interferonsmentioning

confidence: 99%

HPV innate immunity

Craig¹

2002

Front Biosci

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HPV infections of the epidermis and anogenital tract occur frequently in healthy individuals, and 'high risk' HPV types are a major risk factor for cervical cancer. The first line of defense against HPV is the innate immune system, which provides non specific protection against a variety of pathogens and also enhances the adaptive immune response. However, HPV-infected cells often evade innate immune recognition and elimination. HPV gene expression and release of virus occur in superficial squamous cells where virus antigens are not readily detected, and keratinocytes are not lysed during HPV infection so there is no inflammatory response. In addition, HPV early proteins inhibit specific components of the innate immune system. E6 and E7 inhibit signaling by type I interferons and decrease expression of multiple interferon-inducible genes. E5 and E7 inhibit expression of major histocompatibility complex class I proteins on the cell surface. HPV-infected cells are resistant to lysis by natural killer (NK) cells, but are sensitive to cytokine-activated NK cells. Activated macrophages also kill HPV-infected cells and control malignant development. Thus, innate immunity is important for prevention of HPV infections, but HPV often persists due to evasion or inactivation of innate defenses.

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Interferon-αElicits Downregulation of Human Papillomavirus 18 mRNA in HeLa Cells by Selective Repression of Endogenous Viral Transcription

Cited by 11 publications

References 29 publications

Cell-Mediated Immune Response to Human Papillomavirus Infection

Cell-Mediated Immune Response to Human Papillomavirus Infection

The Micro-Immunotherapy Medicine 2LPAPI® Displays Immune-Modulatory Effects in a Model of Human Papillomavirus Type-16 L1-Protein Capsid-Treated Human Peripheral Blood Mononuclear Cells and Antiproliferative Effects in a Model of Cervical Cancer Cells

HPV innate immunity

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